The clinical description of foie gras ducks is illustrated by Dr. Castets, in his thesis presented to the Ecole Nationale Veterinaire de Toulouose (ENVT) in 1979:

At the end of their fattening the animals present the following signs:

• a heavy weight gain (may double)
• Pale skin and mucosas
• A coat " sticky " because of a greasy coating
• Difficulty walking, abdominal ptosis (heavy abdomen) and dyspnea (panting)

Hepatic inflammations linked to steatosis are resumed below:

1. Hepatomegaly
2. Hepatic lesions found during an autopsy of the livers of fattened animals
1. Perihepatitis
2. Hepatic necrosis
3. Circulatory disturbances associated with hypertension
4. Hepatic encephalopathy
5. Global hepatic failure

1. Hepatomegaly
This is the augmentation of the volume of the liver provoked by the accumulation of fat in hepatic cells during the steatosis process. The consequences of hepatomegaly on the overall well being are essentially "mechanic" and include:
- heaviness and abdominal ptosis
- Difficulty walking
- Difficulty breathing (compression of air sacs) accentuated by the absence of a diaphragm in birds

This hepatomegaly is particularly accentuated in ducks starting on the 10th day of the fattening process, and accelerates during the last 3rd of the fattening process.

2. Hepatic lesions encountered during the autopsy

1. Perihepatitis
   "... Inspecting the livers of palmipeds in slaughter and evisceration rooms has shown a noticeable frequent presence of lesions of a perihepatic type. Various microscopic and histologic aspects are described and their sanitary consequences are considered."

   It can be concluded from this study that perihepatic lesions result from inflammatory phenomena linked with:
   - a frequent impairment of respiratory sacs
   - more rarely, an oesophageal perforation during manipulation,
   - finally, a circulatory failure, which may come from pulmonary problems.

   This superficial lesions, at first, (inflammation of the Glisson's capsule) are nonetheless often accompanied by far-reaching impacts on the liver (removed from consumption).

2. Necrosis
   "... After having been reminded of the various types of necrosis observed in the liver, the authors present a series of cases obtained on the livers of fat palmipeds during their preparation in slaughter and evisceration rooms."

   Three hypothesis are remembered in regards to the lesions highlighted here:
   

   1. an infectious origin with a respiratory or digestive origin;
   2. a consecutive toxic origin, either due to the absorption of micotoxins in poor quality corn, either due to nutritional imbalances in individuals ill prepared to the fattening process;
   3. a circulatory origin, consequent to tissular anoxia phenomena of livers at the end of the fattening process.

   3. Circulatory disturbances associated with hypertension

   The modifications to the hepatic structural organization that occur during steatosis are at the origin of the hypertension of the circulatory system, and their consequences are many. During the autopsy, we find animals that present the following:

   • an ascitic liquid in the abdomen,
   • splenomegaly
   • cardiac or renal failure
   These various pathologies may appear alone or with others.

   4. Hepatic encephalopathy

   This is the result of an endogenous intoxication due to the hepatic impairment; the liver can no longer play its role as a circulatory filter. As a result, various metabolites appear in the blood that are usually stopped by the liver (ammonium, mercaptans, short-chain antigens) and that may then reach the central nervous system (particularly sensitive to these compounds) and trigger central nervous troubles such as:

   • cerclage movements,
   • eptileptiform crisis
   • Increase of the intracranial pressure accompanied by migraines, and finally stupor, coma and death.

   5. Hepatic failure

   Beyond the hepatic and perihepatic lesions already evoked, steatosis is part of a global pathologic process which ultimate level is non-reversible and leads to the death of the individual due to hepatic failure.

   Many studies conducted by veterinary services interested in this type of production (they give the names of various studies) notice:

   • the presence of hepatic functional troubles during and at the end of the fattening process,
   • the presence of biochemical modifications associated with these hepatic dysfunctions,
   • the type of hepatic pathology in question.

   This proves that fattened animals develop, to various degrees, depending on their sensitivity, hepatic pathologies provoked by steatosis. Steatosis cannot be considered a normal physiological process; a steatosic liver is indeed a pathologic liver.

   The global inability of the organ to maintain its metabolic functions is evidenced in a very diversifies clinical table associating, or not, metabolic upsets of glucids, lipids, proteins, and water, coagulating problems, secretory problems (gastroenteritis, jaundice, etc...), anemia, ...

   At these levels, steatonecrosis is non reversible and condemns the sick animal to death.